黄芩提取物对脂多糖诱导BV2细胞炎症反应作用及机制探讨

Effects and Underlying Mechanism of Extract of Scutellaria baicalensis Georgi Against LPS-Induced Inflammation in BV2 Cells

目的研究黄芩提取物(SGE)对脂多糖(LPS)诱导BV2细胞炎症反应的作用,并探讨其可能的作用机制。方法四甲基偶氮唑蓝(MTT)法检测细胞存活率;Griess试剂检测细胞上清中NO水平;ELISA法检测细胞上清中白细胞介素(IL)-1β、IL-6、肿瘤坏死因子(TNF)-α水平;Western Blot检测BV2细胞中TLR4蛋白的表达。结果与正常对照组比较,LPS诱导BV2细胞上清中NO、IL-1β、IL-6、TNF-α水平显著增高(P<0.01);与LPS模型组比较,SGE 100μg·m L-1显著降低LPS诱导的BV2细胞上清中炎症因子NO(P<0.01)、IL-1β(P<0.01)、IL-6(P<0.01)、TNF-α(P<0.05)水平。深入研究发现,SGE可显著降低LPS诱导BV2细胞中TLR4蛋白的表达。结论 SGE能够显著抑制LPS所诱导的BV2细胞炎症反应,机制可能与抑制TLR4炎症通路相关。

OBJECTIVE To investigate the anti-inflammatory effects of extract of Scutellaria baicalensis Georgi （SGE） and underlying mechanism by using LPS-induced microglial BV2 cells. METHODS MTT assay was used to observe the cell viability. The content of NO in cell supernatant was measured by Griess reagent. The levels of IL-1β, IL-6 and TNF-α were detected by ELISA kits. The intracellular TLR4 expression was assayed by Western blotting. RESULTS The levels of NO, IL-1β, IL-6 and TNF-α were significantly increased induced by LPS in the supernatant of BV2 ceils （ all P 〈 0. 01 ）. However, co-treatment with SGE 100 μg· mL^- 1 significantly decreased the production of related inflammatory factors including NO （ P 〈 0. 01 ）, IL-1β （ P 〈 0. 01 ）, IL-6 （ P 〈 0. 01 ） and TNF-α （P 〈 0. 05）. Furthermore, SGE significantly inhibited the TLR4 expression induced by LPS in BV2 cells. CONCLUSION SGE is able to alleviate LPS-induced inflammatory responses in BV2 cells through down-regulation of TLR4 protein expression suggesting that SGE has therapeutic potential for the treatment of neuroinflammatory diseases.